Immunological abnormalities during the acute phase of KD are characterized by a marked activation of the immune system: functional activation of monocytes and neutrophils and an excessive production of such inflammatory media tors as cytokines (IL-1, IFN-g, TNF-a), proteases (neutrophil elastase and myeloperoxidase), and toxic oxygen radicals. They can induce EC activation and/or injury. The activated EC increase the expressions of endothelium-leukocyte adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinases-2 and -9 (MMP-2 and -9), vascular endothelial growth factor (VEGF), and its receptor (fms-like tyrosine kinase-1 receptor, flt-1). Furthermore, ECs secrete such soluble molecules as von Willebrand factor, thrombomodulin, intercellular adhesion molecule-1 (ICAM-1), and E-selectin (CD62E), which are secreted from EC into the circulation. However, no specific serological markers of EC damage in KD have been identified so far. Although the presence and titer of anti-endothelial cell antibodies (AECA) has been reported to be correlated with disease activity in systemic vasculitis, pathogenic role of AECA in the pathogenesis of KD vasculitis remains controversial.
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